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The Endocrine System
Endocrine System
Endocrine vs. Exocrine
Organs are not physically connected
Alters activities of target organs/cells
Purpose:
Growth/Development
Reproduction
Regulation
Stress Reactions
Hormones are Activated
By
Hormonal
Humoral
Neural
Gland/Hormone
Functions
Some glands produce >1 hormone
Some hormones produced by >1 gland
Some organs have >1 function
Some hormones have >1 function
Functions of Endocrine
Glands
Endocrine Functions only
Production
Secretion
Contained within other organs which
have other functions
Categories of Glands
Central:
Pituitary
Hypothalamus
Peripheral:
Thyroid
Adrenals
Parathyroids
Thymus
Pineal
Gonads
Pancreas
Others
Hypothalamus
Found on floor of diencephalon
Neural and endocrine functions
Biofeedback mechanism for:
Osmotic pressures
Temperature regulations
Metabolic functions
Pituitary
Extends from Hypothalamus-behind
sphenoid bone
“Master Gland” of body
Anterior- Portal network
Posterior- Neural-contains axons of
Hypothalamus neurons
Anterior Pituitary
GH- Growth Hormone
Prolactin
TSH- Thyroid Stimulating Hormone
ACTH- Adrenocorticotropic
FSH- Follicle Stimulating Hormone
LH- Luteinizing Hormone
Posterior Pituitary
ADH- Anti-Diuretic Hormone
Oxytocin
Pituitary Disorders
Acromegaly- Hypersecretion of GH
Dwarfism- Hyposecretion of GH
Thyroid
Inferior to larynx
2 Lobes
T3- Triiodothyronine
T4- Thyroxine
Calcitonin
Thyroid Disorders
Hypothyroidism- Hyposecretion
Hyperthyroidism- Hypersecretion

Graves Disease
Goiters- iron deficiencies
Parathyroids
4 small glands posterior surface of
thyroid
Parathyroid hormone
Responsible for osteoclast of bone
Decreases blood phosphate levels
(By way of kidneys)
Enhances activation of Vitamin D
Parathyroid Disorders
Hyperparathyroidism
“Moan and groan, stones and bones”
Pineal Gland
Forms part of diencephalon
Melatonin
Inhibits hypothalamus release of
gonadotropins
Melatonin-decreases in light/increase in
dark (circadian rhythm)
Thymus Gland
Posterior to sternum, around great
vessels
Thymosin
Both lymphatic and endocrine
Lymphatic- produces T-lymphocytes
Endocrine- ‘programs’ T-cells
The Adrenals
Located on superior end of each kidney
Medulla- inner gland
Cortex- outer gland
Adrenal Medulla
Sympathetic preganglionic fibers
synapse on cells in medulla
Release of epinephrine/norepinephrine
into general circulation
Adrenal Cortex
Produce over 30 steroid hormones
Three main cortical hormones
Mineralocorticoids
Glucocorticoids
Sex hormones
Mineralocorticoids
Regulate levels of electrolytes and
water in extracellular fluid
95% are aldosterone
Sodium reabsorption
 Potassium excretion

Glucocorticoids
Influence carbohydrate metabolism
Important in body’s response to stress
95% cortisol (hydrocortisone)
stimulates gluconeogenesis
secretion is regulated by ACTH
Sex Hormones
Androgens (testosterone)
Estrogens
Both are secreted in greater numbers
by gonads
Adrenal Disorders
Cushing’s diseasecortisol over-production secondary to
increased ACTH
Addison’s Diseasecortisol/aldosterone deficiencies
Gonads
Testes- males
Testosterone
Ovaries- females
Estrogens
Progesterone
Both produce hormones/gametes
Pancreas
Retroperitoneal-posterior to stomach
Exocrine & Endocrine
Endocrine- islets of Langerhans
Alpha
Beta
Delta
Alpha cells
20% of islets
Hormone glucagon
Stimulates breakdown of glycogen in
liver- raises glucose levels in blood
(glycogenolysis & glyconeogenesis)
Beta Cells
75% of islets
Hormone- insulin
Decreases glucose levels
Glucose Metabolism
Organic components of food:
Carbohydrates (instant-energy)
Glucose
Fats
Fatty acids/glycerols
Proteins
Amino acids
Carbohydrate
Metabolism
Insulin is released by humoral,
hormonal, neural means
Increased glucose
Parasympathetic stimulation
Gastrointestinal hormones
Carbohydrate
Metabolism
60% of carbohydrates are stored as
glycogen in liver
If muscles are not exercised after
eating-stored as muscle glycogen
Glycolysis
Glucose is broken down into pyruvate
and lactate- releasing 2ATPs
(Anaerobic metabolism)
Krebs Cycle
Fat Metabolism
A third of any glucose passing through
liver is converted to fatty acids
Fatty acids are converted to
triglycerides and stored in adipose
tissue
Fat Metabolism
Without insulin, fat is broken back down
into triglycerides/cholesterol  CAD
Fatty acids are also broken down into
ketone bodies
Protein Metabolism
In absence of insulin- protein storage
stops and breakdown begins (muscle)
Amino acid breakdown for energy leads
to increased urea in urine organ
dysfunction
Pancreas Disorders
DiabetesType 1- Juvenile onset
 Type 2- Mature onset
 Gestational diabetes

Type 1 Diabetes
Insulin dependant
S/S:
polyuria
polydipsia
polyphagia
blurred vision
weight loss
Type 2 Diabetes
Generally non-insulin dependant
Has ability to make small amounts of
insulin
Can develop into insulin dependant
Gestational Diabetes
Develops during pregnancy
Deficiencies in insulin leads to inability
to metabolize carbohydrates
Generally disappears after delivery
Insulin Agents
Early- porcine, bovine
Recent- genetic engineered human
insulin
Protein
Rapid, intermediate and long-term
Combination of long-term, rapid each
day
Insulin Types
Regular- Fast acting
0.5-1 hour onset
6-8 hour duration
NPH- Intermediate
1-1.5 hour onset
24 hour duration
Insulin Types
Ultralente- Long acting
4-6 hour onset
36 hour duration
Oral agents:
Diabinese (chlorpropamide)
 Orinase (tolbutamide)
 Micronase (glyburide)
 Glucotrol

Diabetic Emergencies
Hypoglycemia
Hyperglycemia
Diabetic Ketoacidosis (DKA)
Hyperosmolar Hyperglycemic
Nonketotic Coma (HHNK)
Hypoglycemia
Rapid on-set
< 60 mg/dl
Causes:
too much insulin
decreased intake
salicylates
excessive activity
beta blockers
emotional stress
hypothermia
chronic alcoholism
sepsis
S/S of Hypoglycemia
Altered LOCs- irritability, nervousness,
confusion, combative
Cool, clammy
Weak, rapid pulse
Snoring,  salivation
Normal BP
Diabetic Ketoacidosis
Fat metabolism leads to ketoacids
Acidosis leads to  K+ in circulation &
hyperkaluria  K+ deficiency
Osmotic diuresis  dehydration,
electrolyte imbalances
S/S of DKA
Warm, dry skin
Dry mucous membranes
Tachycardia, thready pulse
Postural hypotension
Weight loss
‘Polys’
S/S of DKA
Abdominal pain
Anorexia, nausea/vomiting
Acetone breath
Kussmauls
Decreased LOC
Hyperosmolar
Hyperglycemic
Nonketotic Coma
Generally Type II diabetic
Osmotic diuresis secondary to  sugars
Not acidotic as in DKA
Factors: Geriatric
Preexisting diseases
Increased insulin requirements
Medication use- thiazide, diuretics
Parenteral/enteral feedings
S/S of HHNK
Weakness
Thirst
Polyuria
Weight Loss
Extreme dehydration
Treatment of Diabetic
Emergencies
Hypoglycemia- ABCs
IV- NS
Monitor ECG
Oral, IV Dextrose
Poss. Glucagon IM
Poss. Thiamine
Monitor glucose!
Treatment of Diabetic
Emergencies
Hyperglycemia (DKA, HHNK)ABCs
O2
IV- NS
Monitor ECG for abnormalities